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Heart failure is among the most common causes of morbidity and mortality worldwide and almost half of the patients die from sudden cardiac death, most likely due to ventricular tachyarrhythmias. The current therapeutic strategies for heart failure and arrhythmias are complex and only moderately efficient. In the last decades successful therapies were mainly based on the neurohormonal blockade, including β blockers, ACE inhibitors, angiotensin II receptor AT1 blockers and aldosterone antagonists. However, the lack of benefit of α1-adrenoceptor antagonists, endothelin receptor antagonists and α2-adrenoceptor agonists indicate that the principle of ‘straightforward’ neurohumoural blockade is limited and new strategies are yet to be identified.1 One particular new approach may focus on deciphering the complex interplay between the classical neurohormonal pathways and diverse biologically active peptides during heart failure progression. Indeed, the profile of atrial natriuretic peptide and brain natriuretic peptide (BNP) might offer a new and intriguing target. In particular BNP, which is primarily secreted from the cardiac ventricle upon volume and pressure overload, is a well-established and critical biomarker for risk stratification in heart failure and has various haemodynamic effects such as enhanced natriuresis, vasorelaxation, inhibition of renin-angiotensin system (RAS) and ameliorating cardiac fibrosis (see figure 1).2 The apparent beneficial effects of BNP in opposing RAS overdrive and therefore potentially cardiac remodelling seem to be ideally suited for the development of an effective, rational therapeutic approach.
The first clinical studies conducted in the 1990s showed …
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